The anticonvulsant hypersensitivity syndrome

BACKGROUND: The anticonvulsant hypersensitivity syndrome is a potentially fatal multisystemic reaction to anticonvulsant medications. OBJECTIVES: The purpose of this study was to investigate the clinical characteristics of anticonvulsant hypersensitivity syndrome. RESULTS: A total 32 subjects, aged from 6 to 72 years, diagnosed as having anticonvulsant hypersensitivity syndrome based on clinical and histopathological findings, were included in the study. In 22 of the 32 cases, the anticonvulsants had been administered prophylactically after craniotomy and in 10 cases for epilepsy. When the cases were assessed for skin lesions, maculopapular eruption was registered in 22, Stevens-Johnson syndrome in five, and toxic epidermal necrolysis (TEN) in five. Treatment included suspension of the offending drug and then, except for the cases with toxic epidermal necrolysis, administration of corticosteroids. The 22 cases that required anticonvulsant therapy were treated with valproic acid. In all cases, we observed rapid clinical improvement corroborated by laboratory findings. CONCLUSIONS: It is essential that due importance be given to the development of an eruption in individuals to whom anticonvulsants are administered after craniotomy because anticonvulsant hypersensitivity syndrome is likely to be life-threatening.     

Manifestation of cellulitis after saphenous venectomy for coronary bypass surgery

A few cases of onset of cellulitis after saphenous venectomy for coronary by-pass surgery were first reported by Baddour and Bisno in 1982. We reviewed the dinical characteristics of 31 subjects followed up in our department following onset of manifestations of cellulitis after saphenous venectomy for coronary by-pass surgery. In all the subjects the cellulitis originated at the scar of the saphenous venectomy, and most presented ill-defined, mildly erythematous, slightly oedematous lesions. Mycologically confirmed tinea pedis was found in 25 subjects. All the patients responded well to penicillins or cephalosporins. In this report we comment on the pathogenesis of this complication of saphenous venectomy based on the clinical features of the cases reviewed. We suggest that saphenous venectomy may destroy the lymphatics in the lower leg, that are located adjacent to the great saphenous vein, and thus microorganisms penetrating into the skin may easily cause cellulitis in areas with impaired lymphatic drainage.     

MEDIAL ORBITAL WALL BLOWOUT FRACTURE WITH MEDIAL RECTUS MUSCLE ENTRAPMENT

We report a case of left medial rectus palsy due to entrapment by a fracture of the lateral wall of the ethmoidal sinus following a road traffic accident and discuss the presentation and management of this unusual complication.     

Autoantibodies against platelet glycoprotein Ib in patients with chronic immune thrombocytopenic purpura

The present studies provide direct evidence that some patients with chronic immune thrombocytopenic purpura (ITP) have autoantibodies reactive with platelet glycoprotein Ib ( GPIb ). Microtiter wells coated with a monoclonal antibody that recognized GPIb were reacted with either platelet extract or a control cell extract. After washing and incubating with test plasma, well-bound IgG was quantitated using radioactive anti-IgG. When compared to plasma from normal subjects, plasma from 3 of 106 patients with chronic ITP had significantly increased quantities of IgG bound to microtiter wells reacted with platelet extracts. Negative results were obtained with the remaining 103 patients with chronic ITP and 59 patients with a variety of other platelet disorders. Plasma from two of the three positive patients precipitated a protein from 125I-surface-labeled platelet extract with a molecular weight similar to GPlb . One of the three patients with anti- GPlb antibody also had demonstrable autoantibodies to the platelet glycoprotein llb / llla complex.     

Related binding mechanisms for fibrinogen, fibronectin, von Willebrand factor, and thrombospondin on thrombin-stimulated human platelets

Fibrinogen, fibronectin, von Willebrand factor, and thrombospondin are four large glycoproteins that bind to thrombin-stimulated platelets and influence cellular adhesive functions. The effects of five monoclonal antibodies that react with platelet membrane glycoproteins (GP) IIb and/or IIIa on the binding of these four molecules to stimulated platelets were assessed. Tab and PMI-1, antibodies recognizing GPIIb, had no effect, whereas 10E5 and 2G12, antibodies that immunoprecipitate both GPIIb and IIIa in the presence of calcium, inhibited binding of all four ligands by greater than 85%. T10, an antibody specific for the GPIIb-IIIa complex, produced partial inhibition (60% to 80%) of the binding of each ligand. Inhibitory antibodies were effective in the same dose range for all four proteins and also inhibited binding of fibrinogen, fibronectin, and von Willebrand factor to receptors fixed in an induced state (thrombin-stimulated platelets fixed with paraformaldehyde). Thrombospondin did not bind to these fixed cell preparations. The results suggest that these four adhesive proteins have a related mechanism of binding to thrombin-stimulated platelets. This related mechanism may entail the sharing of some, but not necessarily all, binding sites for the four ligands or a proximal relationship between these binding sites.     

Laparoscopic Features and Repair of a Combined left Spigelian Hernia and left Morgagni Diaphragmatic Hernia

Both Spigelian and Morgagni hernias cause serious morbidity so early diagnosis and timely treatment are necessary. These two types of hernia are more commonly found on the right side of patients. They are rare individually in adults and even rarer in combination. So far, an association between the two hernias has only been reported on the right. We describe the first case of a Spigelian hernia and a Morgagni hernia in a 62-year-old woman, both occurring on the left side. Our accompanying video describes several laparoscopic features that will help lead to early detection and diagnosis.     

Platelet-associated and plasma anti-glycoprotein autoantibodies in chronic ITP

Chronic immune thrombocytopenic purpura (ITP) is due to platelet destruction by circulating antiplatelet antibody. Although autoantibodies against the platelet glycoprotein IIb/IIIa (GPIIb/IIIa) complex and GPIb have been demonstrated using various methods, practical assays for detection of platelet-associated or plasma autoantibodies have not been available. We studied 59 patients with chronic immune thrombocytopenic purpura in whom platelet-associated and plasma autoantibodies against the GPIIb/IIIa complex and GPIb were measured using a newly developed immunobead assay and a previously reported microtiter-well assay. Platelet-associated autoantibody was detected using the immunobead assay in 21 of 28 patients (75.0%; 13 with anti-GPIIb/IIIa, 8 with anti-GPIb). Plasma autoantibodies were noted in 34 of 59 patients (57.6%; 21 with anti-GPIIb/IIIa, 11 with anti-GPIb, and 2 with both). Positive results were noted in 30 of 59 patients using the immunobead assay and in only 14 of 59 using the microtiter-well assay, suggesting that solubilization of the platelets prior to antibody addition, as in the microtiter-well assay, alters epitope stability. Of the 31 thrombocytopenic control patients studied, all gave negative results using both assays. We conclude that these clinically adaptable assays allow detection of autoantibodies in most patients with chronic ITP, confirming the presence of an autoimmune process.